Antibody Inhibition of a Viral Type 1 Interferon Decoy Receptor Cures a Viral Disease by Restoring Interferon Signaling in the Liver

Type 1 interferons (T1-IFNs) play a major role in antiviral defense, but when or how they protect during infections that spread through the lympho-hematogenous route is not known. Orthopoxviruses, including those that produce smallpox and mousepox, spread lympho-hematogenously. They also encode a decoy receptor for T1-IFN, the T1-IFN binding protein (T1-IFNbp), which is essential for virulence. We demonstrate that during mousepox, T1-IFNs protect the liver locally rather than systemically, and that the T1-IFNbp attaches to uninfected cells surrounding infected foci in the liver and the spleen to impair their ability to receive T1-IFN signaling, thus facilitating virus spread. Remarkably, this process can be reversed and mousepox cured late in infection by treating with antibodies that block the biological function of the T1-IFNbp. Thus, our findings provide insights on how T1-IFNs function and are evaded during a viral infection in vivo, and unveil a novel mechanism for antibody-mediated antiviral therapy

Influence of surface structure on corrosion behaviour of welded stainless steel AISI 316L

The work deals with influence of surface finishing on corrosion behaviour of austenitic stainless steel AISI 316L welded by TIG method without filler. Surfaces of the welded stainless steel were modified by mechanical treatment methods (grinding, garnet blasting, chemical method (pickling) and combination of both methods. Experimental procedures included the use of immersion and electrochemical tests where iron chloride (FeCl3) and sodium chloride (NaCl) solutions were used as test electrolytes. The surfaces of the specimens were examined using light microscopy and scanning electron microscopy (SEM). Experimental results confirmed the significant influence of mechanical as well as chemical surface treatment on corrosion behaviour of the welded stainless steel AISI 316L in various chloride solutions

Surface Evaluation of a Multi-Pass Flexible Magnetic Burnishing Brush for Rough and Soft Ground 60/40 Brass

Burnishing is an advanced finishing process that produces higher-quality surfaces with better hardness and roughness than conventional finishing processes. Herein, a flexible magnetic burnishing brush comprising stainless steel pins under permanent magnet poles was used to investigate the influence of multiple passes and directions on the produced surface of soft and rough ground prepared brass. In total, five different samples were burnished on each of the two brass samples prepared. Four samples were processed in the same direction for up to four passes and the fifth sample was processed with two passes in the opposite direction. Results indicate that there was approximately a 30% increase in hardness and an 83% increase in microroughness for rougher-surface brass samples. For smoothly prepared surfaces, there was approximately a 14% increase in hardness and a 35% increase in microroughness. In the same direction of multi-pass burnishing, increasing the number of passes negatively affected surface roughness; for rougher surfaces, the surface hardness reduced and process uniformity increased owing to surface over-hardening and flaking mechanisms, and for smoother surfaces, the hardness, roughness, and process non-uniformity increased with the number of passes owing to repeated surface deformation at some locations and high flaking at other locations. Compared to single-pass burnishing, wherein the surface roughness and microhardness showed almost no change with high process uniformity, in burnishing with two opposite-direction passes, the produced surface exhibited better surface roughness, process uniformity, and microhardness improvements owing to a reverse strain mechanism. Hence, opposite burnishing passes are recommended

Vaccinia Virus Blocks Gamma Interferon Signal Transduction: Viral VH1 Phosphatase Reverses Stat1 Activation

We have analyzed the effects of vaccinia virus (VV) on gamma interferon (IFN-γ) signal transduction. Infection of cells with VV 1 to 2 h prior to treatment with IFN-γ inhibits phosphorylation and nuclear translocation of Stat1 and consequently blocks accumulation of mRNAs normally induced by IFN-γ. While phosphorylation of other proteins in the IFN-γ pathway was not affected, activation of Stat1 by other ligand-receptor systems was also blocked by VV. This block of Stat1 activation was dose dependent, and although viral protein synthesis was not required, entry and uncoating of viral cores appear to be needed to block the accumulation of phosphorylated Stat1. These results suggest that a virion component is responsible for the effect. VV virions contain a phosphatase (VH1) that is sensitive to the phosphatase inhibitor Na(3)VO(4) but not to okadaic acid. Addition of Na(3)VO(4) but not okadaic acid restored normal Stat1 phosphorylation levels in VV-infected cells. Moreover, virions containing reduced levels of VH1 were unable to block the IFN-γ signaling pathway. In vitro studies show that the phosphatase can bind and dephosphorylate Stat1, indicating that this transcription factor can be a substrate for VH1. Our results reveal a novel mechanism by which VV interferes with the onset of host immune responses by blocking the IFN-γ signal cascade through the dephosphorylating activity of the viral phosphatase VH1